scholarly journals Lipoprotein-Associated Phospholipase A2: A Novel Contributor in Sjögren’s Syndrome-Related Lymphoma?

2021 ◽  
Vol 12 ◽  
Author(s):  
Adrianos Nezos ◽  
Charalampos Skarlis ◽  
Anna Psarrou ◽  
Konstantinos Markakis ◽  
Panagiotis Garantziotis ◽  
...  
Keyword(s):  
Protein Expression ◽  
Phospholipase A2 ◽  
B Cell ◽  
Roc Analysis ◽  
Area Under The Curve ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
P Value ◽  
Pla2 Activity ◽  
P Values

BackgroundB-cell non-Hodgkin’s lymphoma (B-NHL) is one of the major complications of primary Sjögren’s syndrome (SS). Chronic inflammation and macrophages in SS minor salivary glands have been previously suggested as significant predictors for lymphoma development among SS patients. Lipoprotein-associated phospholipase A2 (Lp-PLA2)—a product mainly of tissue macrophages—is found in the circulation associated with lipoproteins and has been previously involved in cardiovascular, autoimmune, and malignant diseases, including lymphoma.ObjectiveThe purpose of the current study was to investigate the contributory role of Lp-PLA2 in B-NHL development in the setting of primary SS.MethodsLp-PLA2 activity in serum samples collected from 50 primary SS patients with no lymphoma (SS-nL), 9 primary SS patients with lymphoma (SS-L), and 42 healthy controls (HC) was determined by detection of [3H]PAF degradation products by liquid scintillation counter. Moreover, additional sera from 50 SS-nL, 28 SS-L, and 32 HC were tested for Lp-PLA2 activity using a commercially available ELISA kit. Lp-PLA2 mRNA, and protein expression in minor salivary gland (MSG) tissue samples derived from SS-nL, SS-L patients, and sicca controls (SC) were analyzed by real-time PCR, Western blot, and immunohistochemistry.ResultsSerum Lp-PLA2 activity was significantly increased in SS-L compared to both SS-nL and HC by two independent methods implemented [mean ± SD (nmol/min/ml): 62.0 ± 13.4 vs 47.6 ± 14.4 vs 50.7 ± 16.6, p-values: 0.003 and 0.04, respectively, and 19.4 ± 4.5 vs 15.2 ± 3.3 vs 14.5 ± 3.0, p-values: <0.0001, in both comparisons]. ROC analysis revealed that the serum Lp-PLA2 activity measured either by radioimmunoassay or ELISA has the potential to distinguish between SS-L and SS-nL patients (area under the curve [AUC]: 0.8022, CI [95%]: 0.64–0.96, p-value: 0.004 for radioimmunoassay, and AUC: 0.7696, CI [95%]: 0.66–0.88, p-value: <0.0001, for ELISA). Lp-PLA2 expression in MSG tissues was also increased in SS-L compared to SS-nL and SC at both mRNA and protein level. ROC analysis revealed that both MSG mRNA and protein Lp-PLA2 have the potential to distinguish between SS-nL and SS-L patients (area under the curve [AUC] values of 0.8490, CI [95%]: 0.71–0.99, p-value: 0.0019 and 0.9444, CI [95%]: 0.79–1.00, p- value: 0.0389 respectively). No significant difference in either serum Lp-PLA2 activity or MSG tissue expression was observed between SS-nL and HC.ConclusionsLp-PLA2 serum activity and MSG tissue mRNA/protein expression could be a new biomarker and possibly a novel therapeutic target for B-cell lymphoproliferation in the setting of SS.

Helicobacter Pylori Infection in Sjögren’s Syndrome: Co-incidence or Causality?

2019 ◽  
Vol 15 (3) ◽  
pp. 238-241
Author(s):  
Massoud Saghafi ◽  
Nafiseh Abdolahi ◽  
Reza Orang ◽  
Mohammad Reza Hatef ◽  
Mohammad Hadi Molseghi
Keyword(s):  
Helicobacter Pylori ◽  
Serum Level ◽  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Control Group ◽  
P Value ◽  
H Pylori ◽  
Sjögren‘S Syndrome

Background and Aim: Lymphoid cell infiltration and destruction of exocrine glands, specifically lacrimal and salivary glands are characteristics of Sjogren’s syndrome (SS). An etiological role has been proposed for Helicobacter pylori (H. pylori), interacting in the clinical course and complications of SS (including gastric cancer and lymphoma). The aim of this study was to identify the probable correlation between H. pylori infection and Sjogren’s syndrome (SS). Methods: In this case-control study, ELISA method was used to determine serum level of IgA and IgM anti H. pylori antibody in 43 subjects with SS according to the international criteria and 95 healthy subjects as control. SPSS-17 was used to analyze data with t-test. P value <.05 were considered significant. Results: Serum level of IgM (34.9% vs. 10.5%, p-value= 0.001) and IgA (67.4% vs. 46.3% p value= 0.021) anti H. pylori antibody were significantly higher in SS patients compared to the control group. There was a positive correlation between age and H. pylori infection (r=0.2, Pvalue= 0.05). Conclusion: Patients with SS had a higher prevalence of H. pylori infection compared to the normal population. Eradication of H. pylori is recommended particularly in older patients with SS.

scholarly journals AB0025 B-CELL SUBSETS AS ADDITIONAL DIAGNOSTIC TOOL FOR PRIMARY SJOGREN’S SYNDROME AND SYSTEMIC LUPUS ERYTHEMATOSUS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1315.1-1316
Author(s):  
S. Benevolenskaya ◽  
I. Kudryavtsev ◽  
M. Serebriakova ◽  
I. Grigor’eva ◽  
A. Budkova ◽  
...  
Keyword(s):  
B Cells ◽  
Discriminant Analysis ◽  
B Cell ◽  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Transitional B Cells ◽  
B Cell Subsets ◽  
Sjögren‘S Syndrome

Background:Systemic lupus erythematosus (SLE) and primary Sjögren’s syndrome (pSS) are chronic complex disorders with an autoimmune background, multifactorial etiology, multiple circulating antinuclear antibodies and damage of various organs. SLE and pSS have several similar clinical and serological aspects; likewise, SLE and Sjögren’s syndrome may coexist (so-called secondary Sjögren’s syndrome). However, applied classification criteria do not differentiate SLE and pSS. It is known that humoral immunity plays significant part in pathogenesis of those diseases; hereby, we can expect imbalances in B cell subset frequencies during SLE and pSS.Objectives:To investigate clinical utility of B cell subsets in distinguish SLE and pSS during diagnosis.Methods:A total of 25 SLE patients, 25 SS patients and 49 healthy volunteers (HV) were included in the study. The diagnosis of SLE was performed according to the 2019 EULAR – ACR classification criteria, the diagnosis of pSS - according to the 2016 EULAR – ACR criteria. Phenotyping of blood B cell subsets was done using flow cytometry. Total peripheral blood B cells were identified using CD19 expression, distinct B cell subsets were characterized by IgD, CD38 and CD27 expression. All of the statistical analysis of data was performed with STATISTICA Version 12.0 Inc. (USA).Results:We evaluated the percentages of circulating B-cell subsets using three major classification schemes based on the relative co-expression of either IgD/CD38 (so-called “Bm1-Bm5” classification), IgD/CD27 and CD38/CD27. A discriminant analysis was performed for all B cell classifications. Analysis of CD38 and CD27 co-expression demonstrated most significant separation between patients with SLE and pSS (fig. 1). Moreover, discriminant analysis carried out by using a forward stepwise model demonstrated that the top significance was documented while assessing the percentage of plasmoblasts (CD27hiCD38hi), resting memory B-cells (CD27dimCD38low), mature active B-cells (CD27dimCD38dim), naive mature B-cells (CD27dimCD38low), as well as counting the absolute numbers of transitional B-cells (CD27lowCD38hi), model percent correct was 78,6% (p <0,05, tab.1).Figure 1.Graphic distribution of SLE and pSS patients as well as HV analyzed by discriminant analysis.Conclusion:B cell subsets might provide a useful diagnostic tool for distinction SLE and pSS. More research needed to investigate clinical value of B-cell subsets in autoimmune rheumatic diseases.Table 1.Peripheral B-cell subset composition in SLE and SS patients vs. HV group assessed by discriminant analysis.ParameterF-testp-levelPlasmoblasts (CD27hiCD38hi), %7,93<0.001Resting memory B-cells (CD27dimCD38low), %13,72<0.001Transitional B-cells (CD27lowCD38hi)29,74<0.001Mature active B-cells (CD27dimCD38dim), %5,20<0.001Naive mature B-cells (CD27dimCD38low), %3,100.049Double negative (CD27lowCD38low), %1,980,14Resting memory B-cells (CD27dimCD38low)1,020,36Double negative (CD27lowCD38low)2,320,10Plasmoblasts (CD27hiCD38hi)1,020,36Naive mature B-cells (CD27dimCD38low)1,030,36Mature active B-cells (CD27dimCD38dim)1,020,36Transitional B-cells (CD27lowCD38hi), %1,030,36Disclosure of Interests:None declared

Nodal marginal zone B-cell lymphoma associated with Sjögren's syndrome: A report of three cases

2007 ◽  
Vol 48 (6) ◽  
pp. 1222-1224 ◽  
Author(s):  
Masaru Kojima ◽  
Norihumi Tsukamoto ◽  
Yuri Miyazawa ◽  
Misa Iijima ◽  
Kazuhiko Shimizu ◽  
...  
Keyword(s):  
B Cell ◽  
Sjögren’S Syndrome ◽  
Marginal Zone ◽  
Sjögren's Syndrome ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Sjögren‘S Syndrome

scholarly journals Abnormal B cell response to B cell stimulatory factors (BSF) in patients with Sjögren's syndrome

1987 ◽  
Vol 10 (1) ◽  
pp. 24-30
Author(s):  
Kunio Yamaoka ◽  
Nobuyuki Miyasaka ◽  
Kazuto Satoh ◽  
Masaharu Okuda ◽  
Kusuki Nishioka
Keyword(s):  
B Cell ◽  
Sjögren’S Syndrome ◽  
Cell Response ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Sjögren‘S Syndrome ◽  
B Cell Response

Immunoregulatory effects of dental mesenchymal stem cells on T and B lymphocyte responses in primary Sjögren's syndrome

Immunotherapy ◽  
2022 ◽  
Author(s):  
Deniz Genç ◽  
Burcu Günaydın ◽  
Serhat Sezgin ◽  
Akın Aladağ ◽  
Emine Figen Tarhan
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
B Cell ◽  
Mononuclear Cells ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Primary Sjögren’S Syndrome ◽  
Primary Sjogren’S Syndrome ◽  
Primary Sjögren's Syndrome ◽  
Lymphocyte Responses

Background: In this article, the authors investigate the modulatory effects of dental mesenchymal stem cells (MSCs) on lymphocyte responses in primary Sjögren's syndrome (pSS), which is an autoimmune disease resulting from keratoconjunctivitis sicca and xerostomia. Methods: Mononuclear cells isolated from pSS patients cultured with or without dental MSCs and analyzed for lymphocyte responses via flow cytometry. Results: Dental-follicle (DF)- and dental-pulp (DP)-MSCs downregulated CD4+ T lymphocyte proliferation by increasing Fas-ligand expression on T lymphocytes and FoxP3 expressing Tregs, and decreasing intracellular IFN-γ and IL-17 secretion in pSS patients. DF-MSCs decreased the plasma B cell ratio in the favor of naive B cell population in pSS patients' mononuclear cells. Conclusion: DF- and DP-MSCs can be the new cellular therapeutic candidates for the regulation of immune responses in pSS.

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